NOV 14, 2015
Activation of Tyrosine Kinase to Reduce DME
A small molecule (AKB-9778) that activates a tyrosine kinase receptor (Tie2) could be key in treatment of diabetic macular edema (DME), said Peter A. Campochiaro, MD, during Retina Subspecialty Day on Friday. The rationale behind this study was to supplement anti-VEGF therapy to eliminate edema.
Study design. In a randomized controlled trial, researchers from Johns Hopkins assessed AKB-9778 monotherapy (administered subcutaneously), ranibizumab (RBZ) alone, or RBZ + AKB-9778 in 144 DME patients who received these regimens for 3 months.
Results. They found that AKB-9778 alone did not improve mean central subfield thickness (CST), suggesting that monotherapy is not a viable strategy. However, the RBZ + AKB-9778 group showed significantly greater mean reduction from baseline CST at 3 months compared with RBZ treatment alone (–110 µm vs. –164 µm, p = .008). Dr. Campochiaro also said that 29.2% of patients in the combination therapy group had resolution of edema vs. 17% in the RBZ group.
Side effects. This small molecule was also well tolerated with minimal side effects.—Keng Jin Lee
Financial disclosures. Dr. Campochiaro—Advanced Cell Technology: C; Aerpio: C,S; Alimera Sciences: C; Allergan: C; Applied Genetic Technologies: C; Asclipix: C; Eleven Biotherapeutics: C; Gene Signal: C; Genentech: C,S; Genzyme: S; GlaxoSmithKline: S; Kala Pharmaceuticals: C; Norvox: C; Oxford BioMedica: S; Regeneron: C; Rixi: C; Roche: S,C.
Disclosure key. C = Consultant/Advisor; E = Employee; L = Speakers bureau; O = Equity owner; P = Patents/Royalty; S = Grant support.